Thursday, October 24, 2013

A 50 year old male presented to his physician's office with "heartburn". The physician recorded this ECG, interpreted it as normal, and sent the patient home on an antacid.

See explanation below.

The patient went home and, in front of his wife, he collapsed. He underwent immediate CPR, was found to be in ventricular fibrillation, and was successfully resuscitated. I do not have the post-resuscitation ECG. He underwent coronary stenting (uncertain which artery). He underwent months of rehabilitation and was able to return to work part time.

Could this have been avoided?

1. A 50 year old with "heartburn" is a high risk complaint. There is no way to tell the difference between GI etiology of chest pain and MI. Therefore, even with a normal or non-diagnostic ECG, a 50 year old male patient should undergo serial ECGs and troponins and be admitted to a monitored bed until MI or ACS can be ruled out. This is obviously a very big topic in itself.

2. Did the ECG offer unseen hints? Yes

Leads III and aVF have ST depression with down-up T-waves. Such T-waves are almost always reciprocal to ischemia in the region of aVL (although aVL looks normal here), and in a patient with chest pain are nearly diagnostic of ischemia.The upright portion of the T-wave in aVF is very large compared to the QRS size.

These findings mandate that the patient at least get serial ECGs.

If these remain unchanged, then serial troponins. An emergency cardiac ultrasound could be very useful. And if definitive signs of ischemia develop, the immediate antithrombotic, antiplatelet, and anti-ischemic therapy is indicated, including an immediate angiogram, if symptoms and ECG findings do not resolve.

Lesson:

1. Chest pain should never be assumed to be from a GI source, even if you think the ECG is normal.
2. Ischemia on the ECG can be very subtle and is easily missed. Accurate interpretation requires a lot of skill, practice, and experience. Appreciation of these subtle ECG findings could have helped to avoid a cardiac arrest and its resulting permanent disability
3. Down-up biphasic T-waves are usually reciprocal to up-down biphasic T-waves in the opposing lead and are almost always ischemic
4. T-wave size must be evaluated in the context of QRS size.

15 comments:

Looks to me like there is ST elevation in V1-V3. Was that noticed by the practitioner and they didn't see the reciprocal changes, or is there no ST elevation (sometimes I think there is elevation but have been told by others that there wasn't)

Although its good to understand & detect subtleties,most physicians across the board are more than likely to miss such. The key element is appropriate risk stratification - good clinical history & gestalt especially in such atypical chest pain patients & going through the pathway which would buy you time in investigating & often keeping such patients in short stay units.

I partly agree, but in fact if you only admit and risk stratify patients with NonSTEMI, you will miss many occlusions. 30% of patients who are diagnosed with NonSTEMI have an occluded infarct-related artery at the time of angiography, which is usually more than 24 hours after presentation. These patients have higher mortality, worse EF, and higher biomarkers than NonSTEMI patients with an open artery. Patients with occluded arteries are far more likely to have ECG findings of ischemia, as this patient. We should learn to identify them so that we can get their arteries open. Or at least identify them so that we can do a randomized trial to see if early intervention improves outcomes in these patients.

I think the biggest lesson is that we need to be appropriately conservative with chest pain and its equivalents in the middle-age to elderly patient population.

It takes a TIMI score of 0 with stone-cold normal serial ECGs and biomarkers to get under a 1% miss rate for ACS. Anything other than that is in the low to high single digits for a miss rate, which makes patients like in this example slip through the cracks

I agree, but will repeat what I wrote above. You certainly don't want to miss MI and cardiac arrest, but, even if you admit and patient "rules in" for MI, you also don't want to miss a STEMI-equivalent:

If, in fact you only admit and risk stratify patients with NonSTEMI, you will miss many occlusions. 30% of patients who are diagnosed with NonSTEMI have an occluded infarct-related artery at the time of angiography, which is usually more than 24 hours after presentation. These patients have higher mortality, worse EF, and higher biomarkers than NonSTEMI patients with an open artery. Patients with occluded arteries are far more likely to have ECG findings of ischemia, as this patient. We should learn to identify them so that we can get their arteries open. Or at least identify them so that we can do a randomized trial to see if early intervention improves outcomes in these patients.

Without a previous to compare to, one cannot say for sure. They do not look hyperacute to me: not tall or "fat" enough. If I apply my formula for differentiating the STE of normal variant from anterior STEMI, I get 20.5, which does not indicate LAD occlusion.

Darius,You are of course right. But the first troponin would be negative (in the era of troponin, CK-MB is superfluous). The ECG, on the other hand, is positive and if correctly, read would lead to immediate treatment, before cardiac arrest.Interestingly, the patient's son's name is similar: Dario!Steve Smith

Lead 3 and AVF does shoe an elevated T wave. V5 and V6 looks like something is going on, has a slow heart rate and looks like their is some blockage age.No matter if the patient was complaining of "heartburn", that should have been an alert to draw blood for Troponin level. Heartburn is a sign for a Heart Attack.

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